Hyperbaric oxygen therapy attenuates neuropathic hyperalgesia in rats and idiopathic trigeminal neuralgia in patients.

BACKGROUND: Neuropathic pain after nerve injury is severe and intractable, and current drug and non-drug therapies offer very limited pain relief. Hyperbaric oxygen (HBO 2) has been clinically used for protection of the nervous system after acute injury. We investigated whether HBO 2 treatment could prevent and/or attenuate neuropathic pain in animals and in patients. METHODS: Mechanical allodynia and thermal hyperalgesia and neurochemical alterations of neuropathic pain were analysed in male, adult, Sprague-Dawley rats with sciatic nerve injury. Clinical trials were conducted in patients with idiopathic trigeminal neuralgia. RESULTS: Repetitive HBO 2 treatment [a combination of pressure at 3 atmosphere absolute (ATA) and pure oxygen] greatly inhibited behavioural signs of neuropathic pain manifested as thermal hyperalgesia and mechanical allodynia. Such an HBO 2 treatment also inhibited nerve injury-induced induction of c-Fos and activation of astrocytes and increased phosphorylation of NR2B receptor and the subsequent Ca 2+-dependent signals in rats. Neither high pressure (up to 3 ATA) nor pure oxygen alone resulted in analgesic effect. In clinical trials, one course of HBO 2 therapy (10 consecutive days) produced a rapid-onset, dose-dependent and long-lasting analgesic effects evidenced by the decreased doses of carbamazepine required for keeping patient pain at a minimum and decreased scores of visual analogue scales, which was used for patient's self-evaluation. CONCLUSIONS: These findings support that HBO 2 therapy is an effective approach for treating neuropathic pain in both animals and human beings and suggest that neural protection, anti-inflammation and inhibition of nerve injury-induced altered neural activity may contribute to the analgesic effect of HBO 2 therapy.

Ginsenoside Rg1 enhances endothelial progenitor cell angiogenic potency and prevents senescence in vitro.

This study investigated the effect of ginsenoside Rg1 on the functions of ex vivo cultivated endothelial progenitor cells (EPCs) and whether ginsenoside Rg1 prevented EPC senescence. EPCs isolated from peripheral blood from healthy volunteers were incubated with different concentrations of ginsenoside Rg1 and the effects were observed at different time points. Cell proliferation and in vitro vasculogenesis were assayed and flow cytometry was used to determine the effects of ginsenoside Rg1 on the cell cycle. Senescence and telomerase activity in EPCs were also assayed. It was found that ginsenoside Rg1 promoted EPC proliferation and vasculogenesis in dose-and time-dependent manners. Cell-cycle analysis showed that ginsenoside Rg1 increased the proliferative phase and decreased the resting phase of EPCs. ß-Galactosidase and telomerase activities increased. These results support the view that ginsenoside Rg1 induces EPC proliferation and angiogenesis, and inhibits EPC senescence.

Preparation and characterization of tea polyphenols and vitamin E loaded nanoscale complex liposome.

The purpose of the present work was to prepare nanoscale complex liposome loaded both aqueous soluble drug tea polyphenols (TP) and insoluble drug vitamin E (VE) by reverse-phase evaporation method. The preparation formulation of TP-VE complex liposome was optimized by the orthogonal experiment. The entrapment efficiency of TP was (50.81 +/- 1.91)% while that of VE was (94.05 +/- 3.45)% for the optimal formulation. The results of penetration experiments of TP-VE liposome demonstrated a slight influence of the concentration of TP and the content of cholesterol on the penetration quantity of TP. These results indicate that the complex liposome offers a new approach to entrap aqueous soluble drug and poorly soluble drug, an inner liposome protection, a relatively high drug encapsulation efficiency and a sustained transdermal penetration.